Engineering Photothermal Catalytic CO2 Nanoreactor for Osteomyelitis Treatment by In Situ CO Generation

Abstract Photocatalytic carbon dioxide (CO2) reduction is an effective method for in vivo carbon monoxide (CO) generation for antibacterial use. However, the available strategies mainly focus on utilizing visible‐light‐responsive photocatalysts to achieve CO generation. The limited penetration capability of visible light hinders CO generation in deep‐seated tissues. Herein, a photothermal CO2 catalyst (abbreviated as NNBCs) to achieve an efficient hyperthermic effect and in situ CO generation is rationally developed, to simultaneously suppress bacterial proliferation and relieve inflammatory responses. The NNBCs are modified with a special polyethylene glycol and further embellished by bicarbonate (BC) decoration via ferric ion‐mediated coordination. Upon exposure to 1064 nm laser irradiation, the NNBCs facilitated efficient photothermal conversion and in situ CO generation through photothermal CO2 catalysis. Specifically, the photothermal effect accelerated the decomposition of BC to produce CO2 for photothermal catalytic CO production. Benefiting from the hyperthermic effect and in situ CO production, in vivo assessments using an osteomyelitis model confirmed that NNBCs can simultaneously inhibit bacterial proliferation and attenuate the photothermal effect‐associated pro‐inflammatory response. This study represents the first attempt to develop high‐performance photothermal CO2 nanocatalysts to achieve in situ CO generation for the concurrent inhibition of bacterial growth and attenuation of inflammatory responses.


Figure S2 .
Figure S2.Hydrodynamic size distribution of NNBCs in various incubation solutions for seven days (n = 3).Data are presented as the mean ± SD.

Figure S4 .
Figure S4.The normalized absorbance profile of BTB in different treatment groups.

Figure S7 .
Figure S7.The normalized absorbance profile of CO-Mb in different treatment groups.

Figure S9 .
Figure S9.Principal component analysis (PCA) according to the differentially expressed mRNAs of S. aureus from the control and NNBC + NIR groups.

Figure S10 .
Figure S10.The scatter plot illustrating significantly different genes in the control and NNBC + NIR treatment groups.

Figure S11 .
Figure S11.Gene ontology (GO) pathway enrichment of top 20 down-regulated pathways of S. aureus between control group and NNBC + NIR group.

Figure S12 .
Figure S12.Cellular viabilities of HUVEC and HK-2 cells after cultured with increasing concentrations of NNBCs for (a) 24 h and (b) 48 h (n = 5).Data are presented as the mean ± SD.

Figure S14 .
Figure S14.Principal component analysis (PCA) according to the differentially expressed mRNAs from the control and NNBC + NIR groups.

Figure S15 .
Figure S15.Chord diagram of enrichment analysis of GO from differential expression of genes in NNBC + NIR treated RAW 264.7 macrophages as compared to the control group.

Figure S17 .
Figure S17.Body-weight variations of Balb/c mice after intravenous administration of diverse doses of NNBCs for 15 days (n = 5).Data are presented as the mean ± SD.

Figure S18 .
Figure S18.Hemolysis rate of NNBCs toward red blood cells after 3 h of incubation.DI water acted as a positive control; PBS acted as a negative control (n = 3).Data are presented as the mean ± SD.

Figure S21 .
Figure S21.H&E staining images of major organs (heart, liver, spleen, lung, and kidney) collected from Balb/c mice after intravenous administration of various doses of NNBCs for 15 days (scale bar = 100 μm).

Figure S22 .
Figure S22.Photographs of cutaneous wounds of S. aureus infected mice receiving various treatments.

Figure S24 .
Figure S24.H&E staining images of major organs harvested from the skin wound models after 14 days' treatment (scale bar = 50 μm).